| Autor: |
A H, Mansur, A A, Fryer, M, Hepple, R C, Strange, M A, Spiteri |
| Rok vydání: |
2002 |
| Předmět: |
|
| Zdroj: |
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology. 32(7) |
| ISSN: |
0954-7894 |
| Popis: |
Previously, an association has been reported between an increased risk of asthma and a polymorphism in the Clara cell secretory protein (CC16) gene [namely, an adenine to guanine substitution in the CC16 gene at position 38 (A38G) downstream from the transcription initiation site within the noncoding region of exon 1]. Homozygous individuals for the polymorphic sequence (AA genotype) were reported to have a significant (6.9 fold) increased risk of developing asthma. This finding has not been confirmed independently.To validate the association of CC16 A38G polymorphism to asthma in a separate well-characterized population through a case-control study.We conducted an association study using a sample of 217 unrelated Northern European Caucasians. Individuals were clinically characterized by a validated respiratory questionnaire, spirometry and bronchial reactivity measurement, and genotyped for the A38G polymorphism using PCR and restriction digestion. Association analysis was performed using the nonparametric Chi-squared tests.In the unselected population, 43.3% participants were homozygous for the CC16*G allele and 45.4% were heterozygous (AG). We observed no significant difference in the distribution of positive bronchial reactivity to methacholine (at FEV1 PC20 of/= 8 mg/mL) across the three genotypes. Homozygous individuals for the CC16*A allele did not demonstrate an increased risk of asthma when compared to heterozygous or GG homozygotes. In addition, no significant difference was observed in the distribution of the CC16*A or *G alleles in the asthmatics vs. non-asthmatics.CC16 polymorphism A38G does not influence the predisposition to asthma in this sample. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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